S-Space College of Medicine/School of Medicine (의과대학/대학원) Emergency Medicine (응급의학전공) Journal Papers (저널논문_응급의학전공)
Induced Hypothermia Attenuates the Acute Lung Injury in Hemorrhagic Shock
- Kim, Kyuseok; Kim, Woojeong; Rhee, Joong Eui; Jo, You Hwan; Kim, Kyung Su; Suh, Gil Joon; Singer, Adam J.; Lee, Christopher C.; Kwon, Woon Yong; Lee, Jae Hyuk
- Issue Date
- LIPPINCOTT WILLIAMS & WILKINS
- JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE; Vol.68 2; 373-381
- Hypothermia; Cytokine; NF-kappa B; Glycogen synthase 3 beta; Acute lung injury; Hemorrhagic shock
- Background: In previous animal studies, induction of therapeutic hypothermia (HT) in hemorrhagic shock (HS) had beneficial effects on the hemodynamic and metabolic parameters and on the survival. However, the effect of induced HT on acute lung injury (ALI) in HS has not been investigated. We sought to determine the effects of HT on ALI in HS. Methods: Male Sprague-Dawley rats (350-390 g; n = 8 per group) were randomized to the normothermia (NT; 36-37 degrees C) group or the moderate HT (27-30 degrees C) group and were subjected to volume-controlled (2 mL/100 g weight) HS (90 minutes) followed by 90 minutes of resuscitation. ALI score, lung malondialdehyde content, and myeloperoxidase activity were measured. The expression of glycogen synthase kinase 3 beta (GSK-3 beta), phosphorylated GSK-3 beta, inducible nitric oxide synthase (iNOS), heat shock protein (HSP) 72, and nuclear factor-kappa B (NF-kappa B) in the lung were compared. Results: ALI score, tun malondialdehyde content, and myeloperoxidase were lower in the HT group. GSK-3 beta and iNOS gene expressions in lung tissue were significantly decreased in the HT group (p < 0.05). On the contrary, the expression of phosphorylated GSK-3 beta was increased in the HT group (p < 0.001). HSP 72 was expressed in the HT group but not in the NT group. The activated p65 NF-kappa B levels in lung nuclear extract were significantly lower in the NT group (p = 0.03). Conclusions: HT attenuates HS-induced ALI in rats by the modulation of GSK. HSP 72, iNOS. and NF-kappa B.
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